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肾小球疾病Pathologicalchanges--glomerularinjuryClinicalmanifestations--proteinuria/hematuriaprimaryglomerulardiseasessecondaryglomerulardiseaseshereditaryglomerulardiseasesA.Immunemechanisms(A)depositsofCirculatingImmuno-Complex(CIC)circilationantigen+antibodyCICkidneyCIC/depositsantigenextrinsicdrugs--nonhomologousserum,penicillinfoods—xenogenicproteinpathogen—specificserotypesstreptococci,HBV,HCVintrinsicnucleus（SLE)cytoplasm（ANCA）cellularmembraneantigenoftumorantigenofthyroidWhydoesCICdepositintheglomeruli?(B)insituImmunocomplex1.Nativerenalantigenglomerularbasementmembrane+anti-glomerularbasementmembraneantibody(anti-glomerularbasementmembraneglomerulonephritis)2.AntigenstrappedorplantedDNA+anti-DNAantibody(LupusNephritis)BalancebetweenthedepositandclearanceofICdeterminesthesituationofthediseasesB.Cell-mediatedimmunemechanismsminimalchangeglomerulopathy?C.Non–immunemechanismsglomerularhypertensionhyperlipidemia(LDL-Cho)advancedglycosylationendproducts(protein)glomerulosclerosisInflammationMediatorsofinflammation-activeoxygenandactivenitrogen-lipids-complements-cytokines-chemotaticfactors-adhesionmolecules-growthfactors-vasoactivesubstancesToarouseorpromote-proliferationofcells-accumulationofextracellularmatrix-changesofhistologicalstructure-expressionofimmunomodulatingmoleculesandadhensionmoleculesMechanismsofPrimaryGNimmunenon-immuneinitiationendstagePrimaryGNSitesofpathologicalchangesMesangiumMesangialcellMesangialmatrixBasementmembranePodocyteFootprocessEndothelialcellTheperipheralportionofaglomerularlobulePathologicalchangesBasicalchangesProliferationFibrosisandsclerosisNecrosisInfiltrationofinflammatorycellsExtentsofInjuriesprimaryGNglomerularinjuries—onlyordominatingchangessecondaryGNglomerularinjuries—apartofsystematicdiseasesdiffuseimpairedglomeruli>50%focalimpairedglomeruli<50%globalimpairedcapillaryloopsofaglomerule>50%segmentalimpairedcapillaryloopsofaglomerule<50%Pathological
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